Fig. 2.

STZ-induced diabetes enhances inflammation response, oxidative stress and apoptosis levels in mice subjected to ischemia AKI.

A. Immunohistochemistry and quantitative analysis of TNF-α and F4/80 + macrophages, Scale bars = 100 μm and 50 μm; B. Quantitative real-time PCR detected the mRNA levels of IL-1β, IL6, MCP-1; C. Protein and D. mRNA level of NOX4; E-G. Level of GSH, SOD and MDA; H. Western blot analysis showing the protein expression of cleaved caspase-3; I. Representative micrographs show terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling (TUNEL)-positive cells and proliferating cell nuclear antigen (PCNA) (green nuclei)-positive cells in different groups as indicated; Scale bars = 100 μm; J. The proliferation/apoptosis ratio. Data represent the mean ± S.E.M. for 6–8 mice. *P < 0.05, **P < 0.01, ***P < 0.001 compared to SHAM group; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 compared to ND group; ND: non-diabetic mice; DM: STZ-induced diabetic mice; I/R and DM + I/R: non-diabetic mice and STZ-induced diabetic mice were subject to ischemia reperfusion injury. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)